Sentences with phrase «cell telomeres»

The study, published in the Journal of Investigative Dermatology measured the length of white blood cell telomeres in 1,205 twins from the TwinsUK cohort.

After 13 days, blood was taken to measure the length of their red cell telomeres.

Previous studies have shown that white blood cell telomere length can be predictive of biological aging and is linked with telomere length in other cells in the body.

Some cells have an enzyme that restores telomeres, but in many cells the telomeres shorten over time until the cell loses the ability to divide.

Not exact matches

Variants in the gene called Telomerase Reverse Transcriptase (TERT) on chromosome 5 that were associated with older IEAA were also associated with longer telomeres indicating a critical role for TERT in regulating the epigenetic clock, in addition to its established role of compensating for cell replication - dependent telomere shortening.

These caps shorten every time a cell divides, and short telomeres are a sign that the body's cells are wearing out and ageing.

Studies comparing the telomere length of white blood cells among groups of volunteers show distinct correlations between telomere length and lifestyle.

Whenever chromosomes — the storehouses of our genes — are replicated in preparation for cell division, their telomeres shorten.

In that time, she has uncovered key elements in the biological machinery that prevents telomeres from shortening with each cell division.

Blackburn and Szostak determined that it was a specific DNA sequence in the telomeres that kept chromosomes from fraying whenever they were copied when a cell splits in two.

Telomeres naturally shorten as cells divide, and shortened telomeres are associated in humans with the effects oTelomeres naturally shorten as cells divide, and shortened telomeres are associated in humans with the effects otelomeres are associated in humans with the effects of ageing.

But that imperfect copying also causes the telomeres themselves to be whittled away each time a cell divides.

Although de Lange notes that telomere shortening needs further investigation, she says there's now no doubt that telomeres play a critical role in limiting human cell division and that telomerase can reactivate the process.

The boosted genes had three main beneficial effects: improving the efficiency of mitochondria, the powerhouse of cells; boosting insulin production, which improves control of blood sugar; and preventing the depletion of telomeres, caps on chromosomes that help to keep DNA stable and so prevent cells wearing out and ageing.

And in cancer cells, which unfortunately do not seem to age, telomere length is maintained virtually indefinitely.

Austad recalls one conversation in which Muller made an insightful connection about telomeres, the DNA - and - protein caps at the ends of chromosomes that shorten with every cell division, eventually pushing cells into a nondividing state called senescence.

Telomeres are essential parts of human cells that affect how our cells age.

Working in Berkeley, Lundblad discovered that even without telomerase, yeast cells can sustain their chromosome tips — the first example of an alternative telomere - lengthening pathway.

Each time a cell divides, its telomeres shrink.

After the telomeres had deteriorated, the pair examined the chromosomes in yeast cells closely.

12 Telomeres, sequences of DNA at the tips of chromosomes, get shorter every time a cell divides; when they get too short, the cell dies.

They specifically studied the length of telomeres (repeated DNA sequences) on the ends of chromosomes in leukocytes (white blood cells); the protective caps are believed to be markers of biological aging, because they shrink over time.

Every time linear chromosomes are replicated during late S phase, the DNA polymerase complex is incapable of replicating all the way to the end of the chromosome; if it were not for telomeres, this would quickly result in the loss of vital genetic information, which is needed to sustain a cell's activities.

When your telomeres are finally eaten away after many years, your cells begin to show signs of age, and this process may be a key part of what makes us grow old.

A portion of the telomere DNA is lost during cell division.

In August, 1997, Nobelist Thomas Cech of the University of Colorado at Boulder and colleagues at Geron isolated the human gene for telomerase reverse transcriptase (hTRT)-- an enzyme that reknits loosening telomeres and extends a cell's life.

The team suggests a potential explanation for this observation is that long telomeres enable more rounds of cell division than short telomeres, which could allow cells to live longer and have more opportunities to accumulate carcinogenic mutations.

Researchers have learned that telomeres grow shorter and shorter each time a cell divides; once they're gone, the cell dies.

The key to cancer cell immortality are the cell's telomeres, repetitive stretches of DNA at the ends of chromosomes that may protect the chromosomes when they divide.

And five months later, Jerry Shay and Woodring Wright of University of Texas Southwestern Medical Center, also working with Geron collaborators, published additional findings, showing that, by introducing the hTRT gene to cells, they could make those cells repair unraveling telomeres.

In another clue that cancer cells persist because they maintain their telomeres, those cells that started out with longer telomeres in the experiment lived longer than those with shorter telomeres.

Such a lag time, says Hahn, could allow cancer cells to develop resistance to a drug by finding some other way to maintain their telomeres.

But cells stop dividing and die when telomeres drop below a certain length — a normal part of ageing.

Telomeres, the caps of DNA which protect the ends of chromosomes, shorten every time cells divide.

Located at the ends of chromosomes, telomeres typically shorten with each cell division, until the end of the chromosome becomes so frayed that the cell dies.

It is unclear how the entire body is affected because Spector looked only at telomeres, nucleotides on the ends of chromosomes that slowly erode as cells copy themselves during normal aging.

According to the new theory, the telomeres are short in precancerous cells because telomerase is turned on just enough to maintain but not lengthen the telomeres.

Longer telomeres are integral to cell replication and are associated with longevity.

Previous studies have linked telomeres to the function of mitochondria (essential cell organelles that act as cellular power plants) and vice versa.

Deleting telomere elongation capacity throughout the body would also be life - threatening, because it would mean that our regular proliferating cells (like those in the skin or the lining of the gut) would suddenly have iron limits on their ability to reproduce themselves and thus replenish tissue.

Telomeres shorten every time a cell divides, and ultimately the loss of telomeres leads to cellular senescence, where cells cease to divide, and eventually, ceTelomeres shorten every time a cell divides, and ultimately the loss of telomeres leads to cellular senescence, where cells cease to divide, and eventually, cetelomeres leads to cellular senescence, where cells cease to divide, and eventually, cell death.

When the telomeres get too short, the ends stick to one another, wreaking havoc when the cell divides and in most cases killing the cell.

It also means that the role of telomere biology at a very early step of cancer development is vastly underappreciated,» said senior author Dirk Hockemeyer, a UC Berkeley assistant professor of molecular and cell biology.

The enzyme lengthens the caps, or telomeres, on the ends of chromosomes, which wear off during each cell division.

The reason, he said, is that if a TERT promoter mutation arises to push a precancerous lesion — the mole or nevus — toward a melanoma, the chances are greater in someone with short telomeres that the cell will die before it up - regulates telomerase and immortalizes the cells.

If cells fail to turn up telomerase, they also fail to immortalize, and eventually die from short telomeres because chromosomes stick together and then shatter when the cell divides.

If we introduced stem cells with nice, long telomeres in the first place, we could let them wind down and eventually be lost to apoptosis, senescence, or other sources of damage — and just top our tissues up with more stem cells before enough of those cells were lost to begin to impair tissue function.

So we might just be able to deal with cell loss if we had a sufficiently sophisticated program of stem cell replenishment — using cells engineered to lack the one linchpin function for cancer, namely telomere elongation.

Telomeres at their ends act as caps to prevent biochemical wear and tear, while the cell choreographs the movement of chromosomes by grabbing hold of its centromere handle.

«Two - step process leads to cell immortalization and cancer: Clearer view of the role telomere length and telomerase play in cell immortalization.»